Loading…
Differential interaction of bacterial species from the Burkholderia cepacia complex with human airway epithelial cells
To increase knowledge of the pathogenic potential of the Burkholderia cepacia complex (BCC), we investigated the effects of reference strains of the nine BCC species on human bronchial epithelial cells in vitro. B. multivorans exhibited the highest rates of adherence to and internalization by host c...
Saved in:
Published in: | Microbes and infection 2008, Vol.10 (1), p.52-59 |
---|---|
Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | To increase knowledge of the pathogenic potential of the
Burkholderia cepacia complex (BCC), we investigated the effects of reference strains of the nine BCC species on human bronchial epithelial cells
in vitro.
B. multivorans exhibited the highest rates of adherence to and internalization by host cells. Two out of three clinical isolates recovered from cystic fibrosis patients confirmed the
B. multivorans high adhesiveness. All four
B. multivorans isolates exhibited an aggregated pattern of adherence but any of them expressed cable pili. When bacteria were centrifuged onto cell cultures to circumvent their poor adhesiveness,
B. pyrrocinia exhibited the highest internalization rate, followed by
B. multivorans. The percentages of apoptotic cells in cultures infected with
B. cepacia,
B. multivorans,
B. cenocepacia (subgroups IIIA and IIIB),
B. stabilis and
B. vietnamiensis were significantly higher than in control non-infected cultures. All nine BCC species triggered a similar release of the inflammatory cytokine IL-8, that was not reduced by cell treatment with cytochalasin D. Hence, our data demonstrate, for the first time, that all BCC species exhibit a similar ability to induce the expression of host immune mediators whereas they differ on their ability to adhere to, invade and kill airway epithelial cells. |
---|---|
ISSN: | 1286-4579 1769-714X |
DOI: | 10.1016/j.micinf.2007.10.002 |